Potential neuroprotective effects of 2-hydroxypropyl-? cyclodextrin against amyloid ? (1-42)-induced neurotoxicity on the rat hippocampus

Basit Öğe Kaydı
dc.authoridUyanikgil, Yigit/0000-0002-4016-0522
dc.contributor.authorYalcin, Ayfer
dc.contributor.authorTurunc, Ezgi
dc.contributor.authorKaplan, Mehmet Mahsum
dc.contributor.authorUyanikgil, Yigit
dc.contributor.authorErzurumlu, Yalcin
dc.contributor.authorGavini, Elisabetta
dc.contributor.authorKanit, Lutfiye
dc.date.accessioned2024-08-31T07:49:47Z
dc.date.available2024-08-31T07:49:47Z
dc.date.issued2024
dc.departmentEge Üniversitesien_US
dc.description.abstractThe neurodegenerative mechanisms of Alzheimer's disease (AD) are not fully understood, but it is believed that amyloid beta (A beta) peptide causes oxidative stress, neuroinflammation, and disrupts metabotropic glutamate receptor 5 (mGluR5) signaling by interacting with cholesterol and caveolin-1 (Cav-1) in pathogenic lipid rafts. This study examined the effect of 2-hydroxypropyl-beta-cyclodextrin (HP-CD) on cholesterol, oxidative stress (total oxidant status), neuroinflammation (TNF-alpha), and mGluR5 signaling molecules such as PKC beta 1, PKC beta 2, ERK1/2, CREB, BDNF, and NGF in A beta (1-42)-induced neurotoxicity. The Sprague-Dawley rats were divided into four groups: control (saline), A beta (1-42), HP-CD (100 mg/kg), and A beta (1-42) + HP-CD (100 mg/kg). All groups received bilateral stereotaxic injections of A beta (1-42) or saline into the hippocampus. After surgery, HP-CD was administered intraperitoneally (ip) for 7 days. Cholesterol, TNF-alpha, and TOS levels were measured in synaptosomes isolated from hippocampus tissue using spectrophotometry, fluorometry, and enzyme immunoassay, respectively. The gene expressions of Cav-1, mGluR5, PKC beta 1, PKC beta 2, ERK1/2, CREB, BDNF, and NGF in hippocampus tissue were evaluated using reverse transcription PCR after real-time PCR analysis. Treatment with A beta (1-42) significantly elevated cholesterol, TOS, TNF-alpha, Cav-1, PKC beta 2, and ERK1/2 levels. Additionally, mGluR5, CREB, and BDNF levels were shown to be lowered. HP-CD reduced cholesterol, TOS, and TNF-alpha levels while increasing mGluR5, CREB, and BDNF in response to A beta (1-42) treatment. These findings indicate that HP-CD may have neuroprotective activity due to the decreased levels of cholesterol, oxidative stress, and neuroinflammation, as well as upregulated levels of mGluR5, CREB, and BDNF.en_US
dc.description.sponsorshipOffice of Ege University Scientific Research Projects [12ECZ037, 18ECZ007]en_US
dc.description.sponsorshipThis study was supported by the Office of Ege University Scientific Research Projects (12ECZ037 and 18ECZ007 to A.Y).en_US
dc.identifier.doi10.1080/01480545.2024.2349951
dc.identifier.issn0148-0545
dc.identifier.issn1525-6014
dc.identifier.pmid38726980en_US
dc.identifier.scopus2-s2.0-85192706060en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1080/01480545.2024.2349951
dc.identifier.urihttps://hdl.handle.net/11454/105001
dc.identifier.wosWOS:001217831100001en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofDrug and Chemical Toxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmz20240831_Uen_US
dc.subjectNeurotoxicityen_US
dc.subjectNeuroinflammationen_US
dc.subjectOxidative Stressen_US
dc.subjectGene Expressionen_US
dc.subjectNeuroprotectionen_US
dc.titlePotential neuroprotective effects of 2-hydroxypropyl-? cyclodextrin against amyloid ? (1-42)-induced neurotoxicity on the rat hippocampusen_US
dc.typeArticleen_US

Dosyalar

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayın Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu